Heart failure (HF) is a debilitating, end-stage disease in which abnormal function of the heart leads to inadequate blood flow to fulfill the needs of the body's tissues. Typically, the heart loses propulsive power because the cardiac muscle loses capacity to stretch and contract. Often, the ventricles do not adequately fill with blood between heartbeats and the valves regulating blood flow may become leaky, allowing regurgitation or backflow of blood. The impairment of arterial circulation deprives vital organs of oxygen and nutrients. Fatigue, weakness, and inability to carry out daily tasks may result.
Not all HF patients suffer debilitating symptoms immediately. Some may live actively for years. Yet, with few exceptions, the disease is relentlessly progressive. As HF progresses, it tends to become increasingly difficult to manage. Even the compensatory responses it triggers in the body may themselves eventually complicate the clinical prognosis. For example, when the heart attempts to compensate for reduced cardiac output, it adds muscle causing the ventricles to grow in volume in an attempt to pump more blood with each heartbeat. This places a still higher demand on the heart's oxygen supply. If the oxygen supply falls short of the growing demand, as it often does, further injury to the heart may result. The additional muscle mass may also stiffen the heart walls to hamper rather than assist in providing cardiac output.
Some treatments for HF are centered around medical treatment using ACE inhibitors, diuretics and/or digitalis. It has also been demonstrated that aerobic exercise may improve exercise tolerance, improve quality of life, and decrease symptoms. Cardiac surgery has also been performed on a small percentage of patients with particular etiologies. Although advances in pharmacological therapy have significantly improved the survival rate and quality of life of patients, some HF patients are refractory to drug therapy, have a poor prognosis and limited exercise tolerance. In recent years cardiac pacing, in particular Cardiac Resynchronization Therapy (CRT), has emerged as an effective treatment for many patients with drug-refractory HF.
While CRT does not work for all HF patients, a majority of HF patients are CRT responders, meaning that CRT can be used to improve those patients' HF condition. CRT pacing parameters are preferably individualized for patients to increase CRT benefits.
While echocardiography based techniques are sometimes used to select CRT pacing parameters, echocardiography based CRT pacing parameter selection is very time consuming and poorly reproducible. Device based CRT parameter selection algorithms have alternatively been used to select CRT pacing parameters, including atrioventricular (AV) delay and interventricular (VV) delay. For example, St. Jude Medical's QuickOpt™ algorithm can be used to select AV and VV delays based on measures from an intra-cardiac electrogram (IEGM) or electrocardiogram (ECG), such as P-wave width. However, because QuickOpt™ does not rely on hemodynamic measures, some physicians do not understand and/or trust results of the QuickOpt™ algorithm, although it is quick and easy. Accordingly, the tailoring of CRT parameters for individuals is often not performed for responders and some nonresponders to improve CRT benefits. Additionally, while new multi-electrode leads (MELs), such as St. Jude Medical's Quartet™ left ventricular (LV) lead, provide numerous CRT pacing vector options, most commercially available CRT pacing parameter selection/optimization algorithms (such as QuickOpt™) can not be used to select pacing vectors.
In view of the above, there is still a need for methods, devices and systems that can be used to efficiently identify and select improved Cardiac Resynchronization Therapy (CRT) parameters.